see also:

• Vic DHS patient information sheet - preventing heat stress
• Vic DHS community resources for managing heatwaves
• heat waves
• hyperthermia
• malignant hyperthermia
• hypothermia

• heat illness encompasses a spectrum of severity including:
  • heat oedema
  • heat rash (prickly heat)
  • heat cramps
  • tetany
  • heat syncope
  • heat exhaustion
  • heat stroke
• other causes of hyperthermia include:
  • febrile states due to infections, etc.
  • neuroleptic malignant syndrome (NMS)
  • drugs that increase muscle contraction and thus heat production
    • malignant hyperthermia due to suxamethonium and inhaled volatile anaesthetics
  • radiant heat

• 2-3 million years ago, our human ancestors evolved to be without fur because it gave them one great evolutionary advantage - the newly evolved device of total body perspiration (humans perspire far more than any other animal) becomes much more effective when there is no hair, and a perspiring naked skin can more rapidly lose body heat than any other animal - a great evolutionary advantage in the hot African plains where the human ancestors had evolved to walk upright and walk and run long distances hunting for food. In addition, this added ability to lose heat was essential to ensuring heat protection for the growth in the size of the brain - the human brain gives off ~20W of heat inside an enclosed skull and this needs to be dissipated to prevent brain dysfunction as occurs in heat stroke.
• logically, scalp hair was the only body hair retained en masse as it served to protect the scalp of the erect hominid from the radiant heat of the midday sun, and reduce the brain from over-heating.
• as an aside, from studies on the 3 types of human lice, it appears that after losing their body fur, our ancestors evolved gorilla-hair-like sparse, thick shafted pubic hair not suitable for the grips and limb length of the head louse, and thus the gorilla louse evolved to become human pubic lice, and when we started wearing clothing some 650,000 years ago, the head louse evolved to become a 3rd human louse parasite - the body louse which primarily resides in clothing.

• it is possible to sweat up to 15 litres per day
• thirst does not match all fluids lost by sweating, even if fluids are freely taken
• mild to moderate dehydration increases cardiac work and reduces fluid available for sweating
• even mild dehydration is associated with increased risk of injury, heat stress illness and poorer performance of complex tasks.

• high ambient temperatures
• inability to control environment - clothing, cooling systems, access to water, confined to bed
• dehydration
  • decreased thirst:
    • butyrophenone type antipsychotic agents
    • ACE inhibitors
  • increased fluid losses:
    • exertion
    • heat stress - high temperatures, especially if high humidity, solar radiation, excessive clothing
    • diuretics, alcohol
    • burns
    • vomiting or diarrhoea eg. gastroenteritis
• decreased ability to sweat:
  • ability to lose body heat through perspiration is reduced by:
    • abnormal skin (eg. burns)
    • drugs that impair ability to dissipate heat by impairing perspiration or redistribution of blood to skin
      • anti-muscarinic anticholinergic agents
      • beta adrenergic blockers
      • antihistamines (H1)
      • phenothiazines
    • high humidity
    • clothing
    • inadequate intravascular volume - eg. dehydration
    • neonates
• inability to get blood to the skin to dissipate heat:
  • cardiovascular dysfunction
  • vasoconstrictors
  • inadequate intravascular volume - eg. dehydration
  • hypotension - eg. vasodilators such as nitrates including GTN, calcium channel blockers, antihypertensives
• infants - high metabolic rate, impaired ability to perspire, inability to control environment and care for themselves
• increased heat production
  • febrile illnesses
  • anti-psychotic drugs
  • amphetamines and related psychostimulant substances
  • cocaine
  • hyperthyroidism
• risk factors for exertional heat stress
  • preceding viral infection
  • dehydration
  • fatigue
  • obesity
  • lack of sleep
  • poor physical fitness
  • lack of acclimitization

• defined as a body temperature higher than 41.1°C (106°F) associated with neurologic dysfunction
• HOWEVER, the diagnosis of heatstroke should be considered for patients with altered mental status during environmental heat waves, even in the absence of severe hyperthermia.
• two forms of heat stroke:
  • exertional heat stroke (EHS)
    • generally occurs in young individuals who engage in strenuous physical activity for a prolonged period of time in a hot environment
    • may occur with drug use (eg. amphetamines and related psychostimulant substances or cocaine), strychnine poisoning, thyroid storm and as a complication of status epilepticus
    • tend to have hyperthemia with diaphoresis (ie. sweating)
    • because their ability to sweat remains intact, this group of patients are able to cool down after cessation of physical activity and may present for medical attention with temperatures well below 41°C.
    • prodromal clinical features may include:
      • muscle cramps, nausea, vomiting, diarrhoea, headache, dizziness, weakness, SOB, syncope, bizarre behaviours
  • classic nonexertional heatstroke
    • tend to have hyperthermia with anhidrosis (ie. dry skin), although anhidrosis is late occurrence and may not be present
    • occurs in individuals who lack the capacity to modulate the environment and those at highest risk are infants and elderly persons and patients with diminished cardiovascular reserves are unable to generate and cope with the physiologic responses to heat stress
    • the redistribution of blood flow to the periphery, coupled with the loss of fluids and electrolytes in sweat, place a tremendous burden on the heart, which ultimately may fail to maintain an adequate cardiac output
    • patients with skin diseases and those taking medications that interfere with sweating also are at increased risk for heatstroke because they are unable to dissipate heat adequately
    • occurs during environmental heat waves and is more common in areas that have not experienced a heat wave in many years.
• when therapy is delayed, the mortality rate may be as high as 80%; however, with early diagnosis and immediate cooling, the mortality rate can be reduced to 10%.
• full recovery has been observed in patients with temperatures as high as 46°C, and death has occurred in patients with much lower temperatures.
• body temperatures exceeding 106°F or 41.1°C generally are catastrophic and require immediate aggressive therapy.

• hypoxia and cyanosis may be due to a number of processes, including atelectasis, pulmonary infarction, aspiration pneumonia, Acute Respiratory Distress Syndrome (ARDS) and pulmonary edema
• GIT hemorrhage occurs frequently in patients with heatstroke.
• patients commonly exhibit evidence of hepatic injury, including jaundice and elevated liver enzymes and hypoglycaemia
  • acute liver failure due to centrilobular hepatic necrosis and cholestasis generally occurs in the first 48 hours, but it can peak as long as 2 weeks after the onset of heatstroke.
• rhabdomyolysis occurs in nearly all patients with heat stroke, but particularly those with EHS.
• acute renal failure (acute renal failure (ARF)) occurs in 25-30% of heatstroke patients and may be due to hypovolemia, low cardiac output, and myoglobinuria (due to rhabdomyolysis)
• compartment syndrome is more likely in those with severe rhabdomyolysis
• disseminated intravascular coagulation (DIC) is a rare complication and caries a poor prognosis when it occurs.
• long-term CNS sequelae include cerebellar deficits, dementia, hemiplegia, quadriparesis, and personality changes

• temperature persisting above 39°C despite aggressive cooling measures
• coma duration > 2hrs
• severe pulmonary oedema
• delayed or prolonged hypotension
• lactic acidosis in patients with classic non-exertional heat stroke
• ARF and hyperkalaemia
• high liver enzyme levels during 1st 24hrs

• except for the mildest cases, patients should be admitted to hospital for at least 48hrs to monitor for complications
• ABC's as usual:
  • if unable to protect airway then rapid sequence induction (RSI) for emergency intubation
  • all others should receive supplemental oxygen
  • iv line(s), bedside glucose to exclude hypoglycaemia
  • take bloods FBE, U&E, CK, glucose, LFT's, Ca, PO₄, clotting, DIC screen, |serum lactate, ABG's
    • Rx muscle necrosis-induced hyperkalaemia, hypocalcaemia, hyperphosphataemia on their merits as usual
      • avoid insulin Rx (as risk of hypoglycaemia from liver damage), and calcium Rx (as may increase muscle damage) for hyperkalaemia
      • in the presence of acute renal failure (ARF), may require dialysis
  • iv fluids:
    • although most are dehydrated, aggressive fluid resuscitation generally is not recommended because it may lead to pulmonary edema, and Rx of the hyperthermia may improve hypotension and cardiac function
    • rehydration will depend on pre-existing medical conditions, presence of hypovolaemia, etc.
    • critical patients will generally need a CVP line to assist in determining appropriate fluid replacement
    • hypotensive patients with high CVP may require inotropes, and it seems dobutamine may be the best in this situation as one wishes to avoid cutaneous vasoconstriction of alpha-adrenergic agents.
    • aim for urine output > 3ml/kg/hr to minimise rhabdomyolysis-induced renal failure
• rapid reduction of the core body temperature to 39deg C at a rate of at least 0.2°C/mins the cornerstone of treatment because the duration of hyperthermia is the primary determinant of outcome.
  • insert temperature probe eg. rectal probe for continuous temperature monitoring
  • a thermal instability may persist for a few days, the temperature must be monitored continuously until it is stable.
  • remove clothing
  • spray water on body and use a fan - more comfortable and practical than submersion in ice-water
  • cover the patient with ice water–soaked sheets
  • place ice packs in the axillae and groin
  • cease active external cooling when temp falls to 39deg C to avoid overshooting & iatrogenic hypothermia
  • NB. antipyretics (eg. paracetamol) have no role in heat stroke and may be harmful, exacerbating liver damage
  • NB. dantrolene has not been proven efficacious in Rx of heat stroke
• nil orally
  • may resume oral feeding when mental status, swallowing, and GIT function are normal
• nasogastric tube to monitor for GIT bleed and fluid losses as well as to rest the GIT
• IDC to monitor urine output
• Rx seizures
  • phenytoin is NOT effective in heat stroke-induced seizures, use benzodiazepines or barbiturates instead.
  • if these measures fail, then intubation, paralysis and ventilation, preferably with EEG monitoring may be required
• Rx rhabdomyolysis
• watch for, and Rx disseminated intravascular coagulation (DIC)
• watch for, and Rx Acute Respiratory Distress Syndrome (ARDS) with mechanical ventilation and PEEP
• watch for, and Rx acute renal failure (ARF)
  • in the setting of rhabdomyolysis, mannitol 25-100 g IV infused over 1-2 hr may be the diuretic of choice
• watch for, and Rx compartment syndromes from muscle necrosis
• other investigations
  • CXR
  • ECG
  • CT brain if need to exclude other intracranial cause of altered mental state
  • repeated FBE, U&E, glucose, LFT's, etc as required.

• emedicine